Kidney and Urinary Tract Polyomavirus Infection and Distribution: Molecular Biology Investigation of 10 Consecutive Autopsies

2005 ◽  
Vol 129 (1) ◽  
pp. 69-73 ◽  
Author(s):  
Renzo Boldorini ◽  
Claudia Veggiani ◽  
Diana Barco ◽  
Guido Monga
Keyword(s):  
In Situ Hybridization ◽  
Urinary Tract ◽  
Urinary Bladder ◽  
Renal Pelvis ◽  
Jc Virus ◽  
Hemorrhagic Cystitis ◽  
Kidney Tissue ◽  
Bk Virus ◽  
Human Polyomavirus

Abstract Context.—Distinct human polyomavirus genotypes cause different diseases in patients with renal transplants: BK virus (BKV) causes tubulointerstitial nephritis and ureteral stenosis, whereas both JC virus (JCV) and BKV are responsible for hemorrhagic cystitis. These findings could result from a selective infection of kidney and urinary tract segments by JCV or BKV. Objective.—To verify this hypothesis, 10 complete, unselected, consecutive autopsies from 9 immunocompetent patients and 1 patient affected by acquired immunodeficiency syndrome were investigated. Design.—Samples from kidneys (n = 80), renal pelvis (n = 20), ureter (n = 40), and urinary bladder (n = 30) obtained from 10 consecutive autopsies were investigated by means of multiplex nested polymerase chain reaction to detect polyomavirus DNA and to distinguish different species of the Polyomavirus genus. In situ hybridization and immunohistochemistry were also carried out to define the viral status of the infected tissues. Results.—Polyomavirus DNA was detected in all of the subjects (positive samples ranging from 2 to 7 samples), for a total of 43 of 170 samples (25.3%), distributed as follows: urinary bladder (10/30, 33%), renal pelvis (6/20, 30%), ureter (10/40, 25%), and kidney tissue (17/80, 21%). We found that JCV was most frequently detected overall (23/43 samples, 53.5%) and was also detected most frequently within the kidney (8/17 positive samples, 47%), the renal pelvis (5/6 positive samples, 70%), and the ureter (7/10 positive samples, 70%), whereas BKV was found in 14 samples (32.5%), and it was the prevailing genotype in urinary bladder (6/10 positive samples, 60%). Coinfection of BKV-JCV was found in 6 samples (14%). Immunohistochemistry and in situ hybridization returned negative results. Conclusions.—The viruses JCV and BKV latently persist randomly in kidney and urinary tract. Distinct diseases induced by them could be related more closely to molecular viral rearrangements than to the topographic distribution of latent viruses.

Malakoplakia of the urinary bladder in a young French Bulldog

2021 ◽  
pp. 1-6
Author(s):  
Michael Brückner
Keyword(s):  
In Situ Hybridization ◽  
Urinary Tract ◽  
Urinary Bladder ◽  
Fluorescence In Situ Hybridization ◽  
Urinary Tract Infections ◽  
Bacterial Culture ◽  
Bladder Wall ◽  
Tract Infections ◽  
French Bulldog

Abstract CASE DESCRIPTION A 4-month-old 5.9-kg sexually intact female French Bulldog was presented because of recurrent urinary tract infections in combination with pollakiuria, hematuria, and urinary incontinence. CLINICAL FINDINGS A diagnosis of malakoplakia was made on the basis of results of hematologic and serum biochemical testing, abdominal ultrasonography, bacterial culture, and cystoscopic biopsies of the urinary bladder wall. Biopsy samples were sent for routine histologic examination and fluorescence in situ hybridization to confirm the presence of intracellular and subendothelial bacteria. TREATMENT AND OUTCOME Treatment with enrofloxacin was started after the diagnosis of malakoplakia was confirmed. During treatment, polypoid changes in the urinary bladder decreased dramatically but did not disappear. On follow-up ultrasonography after 12 weeks of treatment, marked improvement was visible and results of repeated bacterial culture and fluorescence in situ hybridization of bladder wall samples were negative. The patient was free from clinical signs and had an ultrasonographically normal urinary bladder 59 weeks after antimicrobial treatment was discontinued. CLINICAL RELEVANCE Malakoplakia, a granulomatous disease characterized by impaired histiocytes that are unable to completely digest phagocytized bacteria, is a very rare disease in dogs, but early suspicion of the condition is essential to allow timely diagnosis and avoid disease progression and the need for prolonged treatment. Malakoplakia should be considered in young dogs with chronic urinary tract infections; the diagnosis can be made through a combination of histologic examination and fluorescence in situ hybridization of bladder wall biopsy samples.

scholarly journals Renal and urinary findings in 20 patients with Williams-Beuren syndrome diagnosed by fluorescence in situ hybridization (FISH)

2004 ◽  
Vol 59 (5) ◽  
pp. 266-272 ◽  
Author(s):  
Sofia Mizuho Miura Sugayama ◽  
Vera Hermina Kalika Koch ◽  
Érica Arai Furusawa ◽  
Cláudio Leone ◽  
Chong Ae Kim
Keyword(s):  
In Situ Hybridization ◽  
Urinary Tract ◽  
Fluorescence In Situ Hybridization ◽  
Chromosome Region ◽  
Voiding Cystourethrogram ◽  
High Incidence ◽  
Hybridization Test ◽  
A Prospective Study ◽  
Elastin Gene

PURPOSE: Williams-Beuren syndrome is a rare multiple anomalies/mental retardation syndrome caused by deletion of contiguous genes at chromosome region 7q11.23. The aim of this work was to determine the frequency and the types of renal and urinary tract anomalies in 20 patients with Williams-Beuren syndrome. METHODS: The fluorescence in situ hybridization test using a LSI Williams syndrome region DNA probe was performed for all 20 patients to confirm the diagnosis of Williams-Beuren syndrome. A prospective study was performed in order to investigate renal and urinary aspects using laboratory assays to check renal function, ultrasonography of the kidneys and urinary tract, voiding cystourethrogram and urodynamics. RESULTS: Deletion of the elastin gene (positive fluorescence in situ hybridization test) was found in 17 out of 20 patients. Renal alterations were diagnosed in 5 of 17 (29%) the patients with the deletion and in 1 of 3 patients without the deletion. Fourteen patients with the deletion presented dysfunctional voiding. Arterial hypertension was diagnosed in 3 patients with deletions and 1 of these presented bilateral stenosis of the renal arteries. CONCLUSIONS: Due to the high incidence of renal and urinary abnormalities in Williams-Beuren syndrome, performing a systematic laboratory and sonographic evaluation of the patients is recommended.

Expression and localization of epithelial sodium channel in mammalian urinary bladder

1998 ◽  
Vol 274 (1) ◽  
pp. F91-F96 ◽  
Author(s):  
Peter R. Smith ◽  
Scott A. Mackler ◽  
Philip C. Weiser ◽  
David R. Brooker ◽  
Yoon J. Ahn ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Urinary Bladder ◽  
Mrna Expression ◽  
Northern Blot ◽  
Apical Membrane ◽  
Bladder Epithelium ◽  
Rat Urinary Bladder ◽  
Luminal Membrane ◽  
Electrophysiological Studies

The mammalian urinary bladder exhibits transepithelial Na+ absorption that contributes to Na+ gradients established by the kidney. Electrophysiological studies have demonstrated that electrogenic Na+ absorption across the urinary bladder is mediated in part by amiloride-sensitive Na+ channels situated within the apical membrane of the bladder epithelium. We have used a combination of in situ hybridization, Northern blot analysis, and immunocytochemistry to examine whether the recently cloned epithelial Na+ channel (ENaC) is expressed in the rat urinary bladder. In situ hybridization and Northern blot analyses indicate that α-, β-, and γ-rat ENaC (rENaC) are expressed in rat urinary bladder epithelial cells. Quantitation of the levels of α-, β-, and γ-rENaC mRNA expression in rat urinary bladder, relative to β-actin mRNA expression, indicates that, although comparable levels of α- and β-rENaC subunits are expressed in the urinary bladder of rats maintained on standard chow, the level of γ-rENaC mRNA expression is 5- to 10-fold lower than α- or β-rENaC mRNA. Immunocytochemistry, using an antibody directed against α-rENaC, revealed that ENaCs are predominantly localized to the luminal membrane of the bladder epithelium. Together, these data demonstrate that ENaC is expressed in the mammalian urinary bladder and suggest that amiloride-sensitive Na+ transport across the apical membrane of the mammalian urinary bladder epithelium is mediated primarily by ENaC.

The Characteristics of Hemorrhagic Cystitis After Allogeneic Stem Cell Transplantation, and Possible Predictive Value of Absolute Lymphocyte Count for Clinical Outcome.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1284-1284
Author(s):  
Seung-Ah Yahng ◽  
Byung-Sik Cho ◽  
Sung-Eun Lee ◽  
Ki-Seong Eom ◽  
Yoo-Jin Kim ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Lymphocyte Count ◽  
Advanced Disease ◽  
Jc Virus ◽  
Hemorrhagic Cystitis ◽  
Disease Status ◽  
Absolute Lymphocyte Count ◽  
Bk Virus ◽  
P Value ◽  
Incidence Risk

Abstract Abstract 1284 Background; Hemorrhagic cystitis (HC) after allogeneic stem cell transplantation (SCT) is a common complication associated with frequent prolongation of hospitalization and occasional death and yet, the observed risk and prognostic factors as well as the understanding of pathophysiology remain inconsistent. Recent evidences point to HC being triggered by reactivation of viral replication, mainly BK virus, implicating factors standing for recipients’ status of immunity may correlate with the incidence, severity and prognosis of HC. Methods; We retrospectively investigated 450 adult patients who underwent allogeneic SCT from January 2007 through December 2009 in order to analyze the incidence, risk and prognostic factors of HC. Results; The median age was 38 years old (range, 15–70) and 90 % of the patients had malignant disease. Thirty-five percent of patient (n=159) had advanced disease status at transplantation. Two hundred thirty-nine patients (53%) and 211 (47%) had related and unrelated donors, respectively. Conditioning regimens consisted of myeloablative (n=266, 59%) and reduced-intensity regimens (n=184, 41%). With a median follow-up of 549 days (range, 83 – 1172), 58 patients developed HC (cumulative incidence, 13.2%±1.6%) and the median day of onset was 36 days after transplant (range, 1–441) consisting of pre-engraft (n=13) and post-engraft HC (n=45). Among 58 patients with HC, urine virus was detected in 54 patients. Thirty patients had positive PCR for BK virus and 19 patients were positive by JC virus PCR. Not all the patients with positive PCR results showed growth by urine culture. Eleven patients were BK virus culture positive and 7 patients showed growth of adenovirus. Four patients showed positive PCR results for both BK virus and JC virus. The overall severity of HC was as follows; grade I (19%), grade II (21%), grade III (47%), and grade IV (14%). On multivariate analyses, advanced disease status at transplantation [HR (95% CI), 1.81 (1.003-3.266), P-value=0.049] and concurrent acute graft-versus-host disease (GVHD) [HR (95% CI), 1.88 (1.013-6.487), P-value=0.046] were revealed to be significantly associated with the occurrence of HC. All patients with HC were initially treated with forced hydration and/or bladder irrigation, and cidofovir at 5 mg/kg/day for two consecutive weeks and biweekly thereafter was used in 18 patients with documented test results associated with BK virus showing no improvement within 7 days after treatment. In 4 cases of grade IV HC with urinary tract obstruction, double-J catheterization or percutaneous nephrostomy were performed. The overall complete response (CR) rate of HC patients was 72%. Notably, multivariate analyses showed that patients with absolute lymphocyte count over 1000/μL at onset of HC had significantly better outcome in the achievement of CR [HR (95% CI), 10.8 (1.16-100.81), P-value=0.036)]. Conclusions; This study demonstrates the incidence, risk and prognostic factors of 58 patients with HC, and the value of the absolute lymphocyte count at onset of HC as a prognostic predictor. Patients who have advanced disease status at transplantation or develop acute GVHD are at high risk of developing HC, and early monitoring should be implemented. Our data also indicates that replication of JC virus as well as BK virus may account for a considerable portion of etiologies of HC. Prospective trials on analyzing the risk and prognostic factors for HC are needed for the development of reliable tools for predicting HC, and the relation between degree of immune reconstitution or JC virus and the occurrence of HC after SCT should also be further investigated. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Analysis of 15 novel full-length BK virus sequences from three individuals: evidence of a high intra-strain genetic diversity

2004 ◽  
Vol 85 (9) ◽  
pp. 2651-2663 ◽  
Author(s):  
Yiping Chen ◽  
Paul M. Sharp ◽  
Mary Fowkes ◽  
Olivier Kocher ◽  
Jeffrey T. Joseph ◽  
...  
Keyword(s):  
Striated Muscle ◽  
Jc Virus ◽  
Regulatory Region ◽  
Bk Virus ◽  
Full Length ◽  
Human Polyomavirus ◽  
Coding Region ◽  
Nucleotide Substitutions ◽  
Source Of Infection

To determine the variability of BK virus (BKV) in vivo, the sequences of nine full-length molecular clones from the striated muscle and heart DNA of a patient with BKV-associated capillary leak syndrome (BKVCAP), as well as three clones each from the urine of one human immunodeficiency virus type 2-positive (BKVHI) and one healthy control subject (BKVHC), were analysed. The regulatory region of all clones corresponded to the archetypal regulatory region usually found in urine isolates. Analysis of the predicted conformation of BKVCAP proteins did not suggest any structural differences on the surface of the viral particles compared with BKVHI and BKVHC clones. No amino acid changes common to most BKVCAP clones could be identified that have not already been reported in non-vasculotropic strains. However, the coding region of each clone had unique nucleotide substitutions, and intra-host variability was greater among BKVCAP clones, with a mean difference of 0·29 % per site compared with 0·16 % for BKVHI and 0·14 % for BKVHC. The clones from each strain formed monophyletic clades, suggesting a single source of infection for each subject. The most divergent BKVCAP clones differed at 0·55 % of sites, implying a rate of nucleotide substitution of approximately 5×10−5 substitutions per site per year, which is two orders of magnitude faster than estimated for the other human polyomavirus, JC virus.

JC virus infection and Alzheimer's disease: Reappraisal of an in situ hybridization approach

1992 ◽  
Vol 31 (4) ◽  
pp. 439-441 ◽  
Author(s):  
Outi Heinonen ◽  
Stina Syrjänen ◽  
Rauno Mäntyjärvi ◽  
Kari Syrjänen ◽  
Paavo Riekkinen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
In Situ Hybridization ◽  
Virus Infection ◽  
Jc Virus
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